Redox TRPs in diabetes and diabetic complications: Mechanisms and pharmacological modulation

Abstract

Transient receptor potential (TRP) channels have shown to be involved in a wide variety of physiological functions and pathophysiological conditions. Modulation of TRP channels reported to play a major role in number of disorders starting from central nervous system related disorders to cardiovascular, inflammatory, cancer, gastrointestinal and metabolic diseases. Recently, a subset of TRP ion channels called redox TRPs gained importance on account of their ability to sense the cellular redox environment and respond accordingly to such redox stimuli. Diabetes, the silent epidemic of the world is increasing at an alarming rate in spite of novel therapeutic interventions. Moreover, diabetes and its associated complications are reported to arise due to a change in oxidative status of cell induced by hyperglycemia. Such a change in cellular oxidative status can modulate the activities of various redox TRP channels (TRPA1, TRPC5, TRPMs and TRPV1). Targeting redox TRPs have potential in diabetes and diabetic complications like neuropathy, cardiomyopathy, retinopathy, cystopathy, and encephalopathy. Thus in this review, we have discussed the activities of different redox sensing TRPs in diabetes and diabetic complications and how they can be modulated pharmacologically, so as to consider them a potential novel therapeutic target in treating diabetes and its comorbidity.

Keywords: 2-aminoethoxydiphenyl borate (PubMed CID: 1598); Adenosine diphosphate ribose (PubMed CID: 30243); Allyl isothiocyanate (PubMed CID: 5971); Capsaicin (PubMed CID: 1548943); Capsazepine (PubMed CID: 2733484); Diabetes; Diabetic complications; HC030031 (PubMed CID: 5754); ML204 (PubMed CID: 230710); N-(p-amylcinnamoyl) anthranilic acid (PubMed CID: 5353376); Oxidative stress; Redox TRP channels; Resiniferatoxin (PubMed CID: 68029831); TRP channels; Waixenicin A (PubMed CID: 73755210)..